MiR-24 enhances radiosensitivity in nasopharyngeal carcinoma by targeting SP1.

Min Kang,Jun Wang,Pingting Zhou,Rensheng Wang,Tingting Zhao,Tingting Wei,Jingjian Xiao

doi:10.1002/cam4.660

Abstract

Radioresistance remains a major problem in the treatment of patients suffering from nasopharyngeal carcinoma (NPC). A better understanding of the mechanisms of radioresistance may generate new strategies to improve NPC patients' responses to therapy. This study was designed to investigate the effect of microRNA on the radiosensitivity of NPC cells. A microRNA microarray indicated that miR‐24 was downregulated in NPC cell lines and tissues. Furthermore, cell proliferation was suppressed and radiosensitivity increased when miR‐24 was ectopically expressed in NPC cells. Specificity protein 1 (SP1) was additionally verified as a direct functional target of miR‐24, which was found to be involved in cell viability as well as the radiosensitivity of NPC cells. In conclusion, the results of this study suggest that the miR‐24/SP1 pathway contributed to the reduction in radioresistance in human NPC and that it may thus represent a therapeutic target.

Highlights

Nasopharyngeal carcinoma (NPC) is a type of cancer derived from epithelial cells located in the nasopharynx [1]
When we applied qRT-PCR analysis on expression of miR-24 and Specificity protein 1 (SP1) in tumors treated with radiation therapy, the results showed an increase in levels of miR-2 4 (Fig. 4B) and a decrease in SP1 levels mRNA compared with untreated tumors (Fig. 4C)
We observed that miR-2 4 is frequently downregulated in NPC cell lines and freshly frozen clinical specimens

Summary

Introduction

Nasopharyngeal carcinoma (NPC) is a type of cancer derived from epithelial cells located in the nasopharynx [1]. MicroRNAs (miRNAs) are one type of small noncoding RNAs (20–24 nucleotides) which posttranscriptionally modulates gene expression through negative regulation of the stability or translational efficiency of their target mRNAs [4, 5]. These effects are obtained by miRNA binding to the 3′-untranslated region (3′UTR) of their target mRNAs, which can reduce the expression of the associated protein. A number of studies have shown that miRNAs can function as either oncogenes or tumor suppressors to regulate all kinds of basic cellular functions, including proliferation, migration, differentiation, apoptosis, cell cycle, and angiogenesis, and

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